ABSTRACT
The dopamine biosynthetic machinery of intact synaptosomes of rat striatum showed a 5-fold increase in development from 3-day-old neonates to adults, and it was fully developed between 2-3 weeks after birth. Concurring with this development was the appearance 2 weeks after birth of a regulatory mechanism(s) through which amphetamine in vivo induced an inhibition of dopamine biosynthesis. The inhibition was not appreciably reversed when haloperidol, in addition to amphetamine, was administered.
Subject(s)
Corpus Striatum/metabolism , Dextroamphetamine/pharmacology , Dopamine/biosynthesis , Aging , Animals , Animals, Newborn , Corpus Striatum/enzymology , Depression, Chemical , Haloperidol/pharmacology , Rats , Synaptosomes/metabolism , Tyrosine 3-Monooxygenase/metabolismABSTRACT
Subcellular studies of choline uptake of rat striatum indicated a correspondence between the Na(+)-dependent uptake and choline acetyltransferase (ChAc), whereas there was a lack of correspondence between the Na(+)-independent uptake and ChAc. Subcellular studies also showed a correspondence between the Na(+)-dependent uptake and hemicholinium-3 inhibition, and more important, particles that accumulate choline were shown to consist of at least two subcellular populations. A comparison was made of kinetic data from three areas of the rat brain: corpus striatum, cerebral cortex, and hypothalamus. Taken together, our data on choline uptake give added support to the idea that the Na(+)-dependent choline transport is concentrated in the striatum and specifically related to cholinergic nerve endings. Morphine and methadone in vitro inhibited the Na(+)-dependent choline uptake. In vivo morphine induced a significant lowering of theV max in the rat cerebral cortex, but not in the striatum. This finding is consistent with the known action of morphine on acetylcholine turnover.
